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                                         Coronary arteries are the major site for human atherosclerosis .CAD is considered the ultimate determinant of  cardio vascualr health of our global population.Coronary atherosclerosis has a predilection for proximal sites and branching points.Typically it occurs in leftmain, LAD ostium, LCX ostium, proximal LAD, diagonal origins, OMs RCA  and its branches .

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Septal branches , even though divide very early  from the LAD , it  is  uncommon  to get affected by coronary atherosclerosis.  Even for an experienced   interventional cardiologist  , it  would be very rare to have  performed a  PCI for septal disease.

Why septal branches of LAD is rare to suffer from atherosclerosis ?

We don’t know the answer yet.

But , it is thought,septal branches are near perpendicular branches .The branching angle and incidence of atherosclerosis has a peculiar relationship.IAt any bifurcation  point , the atherosclerosis tend to occur ,  if the angle is more acute , and is  less common in abtuse angles .It is  almost rare  ,  if branching happens at   exact  90 degree angle or so !

The other reason for septal branches being immune to atherosclerosis is  , it runs within the muscle in its major course. The constant squeezing action(. . . and possibly bridging also)  makes it difficult for the  process of atherosclerosis to sustain and grow .

Can you still get a  septal CAD ?

Yes,  usually as  a component of bifurcation or trifurcation lesion. Some times a diagonal and septal are very close together and  atherosclerosis involves  both ostia.

What is  the implication for the  cardiologist to perform  a PCI with stenting in a septal branch of LAD  ?

PCI and stenting in the septal branches are more prone for crushing and fracture   as it is constantly exposed to the mechanical effects of muscle contraction.

Any other significance for septal branches of LAD ?

  • Isolated septal myocardial infarction can occur.This could be even a embolic manifestation.
  • Septal branches of LAD are potential target for therapeutic embolisation (By injecting alcohol)  in patients  with hypertrophic obstructive cardiomyopathy(HOCM) .This manover aims to produce a controlled septal myocardial infarction and thus paralysing the left ventricular outflow tract and reduce the dynamic LVOT gradient. This form of treatment, was glorified till recently now considered experimental !

Contrary to popular belief ,great things happen only rarely in medicine . It takes  only  few  months of  training  or  workshops ,  for a  wrong or inappropriate concept  to  percolate  our  brains !  But , it  would require,   decades  of  time , energy  and  efforts  ,  for  correcting  that  wrongly  assimilated concept  in medicine !

Interventional cardiologists are  among the  rare breed of physicians,   who always believe in evidence !  But ,  the quality of  the  evidence  is rarely questioned  !  30 years of PCI  & 20 years of stenting has failed  our  common senses ! Fortunately , today,  we have 135 pages of new evidence ( Not really new , old evidence interpreted with  sound logic !)

Hats off to ACC and associates for bringing out this much belated appropriateness guidelines for the interventional cardiologists.

ACCF/SCAI/STS/AATS/AHA/ASNC 2009 Appropriateness Criteria for Coronary Revascularization

A Report of the American College of Cardiology Foundation Appropriateness

Criteria Task Force, Society for Cardiovascular Angiography and Interventions,

Society of Thoracic Surgeons, American Association for Thoracic Surgery,

American Heart Association, and the American Society of Nuclear Cardiology

Endorsed by the American Society of Echocardiography, the Heart Failure Society of America, and the

Society of Cardiovascular Computed Tomography

Click here to get guidelines

http://circ.ahajournals.org/cgi/reprint/CIRCULATIONAHA.108.191768v1.pdf

If you don’t have time to read the entire document (135 pages  )

Just remember only one point

Common sense,  more  often  prevails  over  evidence ,  in medicine . Apply it  , frequently  in your patients .They will reep the benefits !

Drug eluting stents : A slap on the face of Evidence based cardiology . . .

Click the BMJ link or read below

 

venkat-bmj

It is often said science is sacred and unfortunately we forget ,  science is not a heavenly creation and it is the creation of scientist of varying grades of integrity fueled by the vested interest of medical industry . It has been a almost a daily affair , some of the devices and drugs are recalled or found to be unsafe on patients.

Now the big cat has come out .The Drug eluting stent has fallen from Hero to Zero in a short span of 5 years. It was projected to have zero percent restenosis in 2002 . And now we realize it is Zero percent truth.

What has started as anecdotal reports of late stent thrombosis has indeed become an epidemic in all DES patients. The five studies that has been published in the NEJM this month (March 2007) has convincingly proved how unsafe these stents are in most of the coronary population .

Millions of patients in whom this stent was implanted will carry an impending stent thrombosis and possibly an SCD . Who is to take care of them ?

The DES story is a clear cut case of getting premature approval for a dangerous form of treatment inside human coronary arteries.

It is amazing how the scientist’s eyes are shut by the illusion of knowledge and lure of wealth. How foolish they were to think drug which was administered via the stent will selectively prevent vascularisation and leave the normal endothelium intact . Now they realized , one should not suppress the endothelial growth around the stent and got the fundamental point wrong. Which was the key reason for the astonishing episodes of late stent thrombosis. When we play with biology of nature we have to be little more careful .God has created man and his heart for over a million years . One can not alter it by a 6 month follow up study of DES .

When ICDs were exposed last year , of similar disastrous outcome they were recalled and explanted . How are we going to unstent the millions of coronary arteries ?

Somewhere along the line the medical professionals have lost the battle against the Wall street and NASDAQ . Or how else we can explain repetition of similar events.

The wages for the modern technology , the patients have to pay a heavy price.

Let us all hope common man with common sense will reign supreme over the sixth sense of the uncommon man . . .

“Ignorance is better than illusion of knowledge”

Dr Venkatesan Sangareddi MD , Assistant Professor of cardiology , Madras medical college Chennai, India

Anginal pain is a type of visceral pain.It is carried by type  C  unmylinated  nerve fibres.The perception of angina is a complex process.It is a combination of visceral and cutaneous referral pain.

How often is angina silent in diabetes mellitus ?

Presence of  diabetes per se does not make an angina silent. In fact,  if  one takes 100 patients with diabetes  , if angina occur in them , it is more often  , manifest than silent. So , only few of  the  diabetic patients who develop diabetic autonomic neuropathy fail to have angina.The exact incidence is not known.It could be around 20%.

If angina can be silent in diabteics , can they have anginal equivalents ?

This again is not answered in literature. Among the anginal equivalents , the most common is  dyspnea , which  can occur in diabetics.But now , we know dyspnea also needs thoracic nerve signals  from the intercostal muscle spindle and colgi organs.This can also be impaired in diabetics.

Can silent and mainfest episodes occur in a same  patient  ?

Yes.

Once silent does not mean always silent, and similarly once angina is felt it  does not mean he is going to feel the next episode as well !

This  strongly reminds us medical science  is  much a complex  subject and what we know is very little in pain perception.

How is silent ischmia different from silent angina ?

There is considerable  overlap  between  silent ischemia and silent angina

The questions to be answered are 

Which is silent  ?  Is it the angina or is it the ischemia or both ?

Silent ischemia can occur in any individual ,  this is also called as silent CAD . When  ischemia occurs  but  fails  to generate pain it is silent ischemia .Undiagnosed  CAD in asymptomatic individuals is also called silent ischemia or CAD.In this population  Exercise stress testing detects  CAD which was otherwise silent and masked.These patients may develop angina during EST.

During exercise stress testing many times patient has significant ST depression  more than 2mm but still chest pain may not occur.These episodes may either be silent ischemia or  ngina. Many times the EST is terminated before angina is manifest .( Chest pain is the last to occur in the chain of events following ischemia- Concept of ischemic cascade )

What are the other situations where angina can be silent ?

  • Pain perception  and threshold  level is  high ,  so patient indeed has anginal  signals but fails to feel it .
  • Patients on  antianginal medication , fail to feel the angina.
  • Chronic betablocker therapy can exactly mimic  autonomic neuropathy

Is it a blessing for the patient  to have painless episodes of angina ? 

When their  ischemic colleagues , suffer a lot with chest pain it is tempting to think these diabetic patients  are blessed!

Scientifically , this could be true in at least in  some  especially in a patients  who’s coronary anatomy is known  and devoid of any critical proximal lesions. For example a small PDA  lesion can produce  severe angina  , but may be silent  in diabetic and be comfortable .This lesion is  insignificant other wise * !

It should  also be recalled , pain relief has been an important goal for treatment  of CAD .In olden days,  thoracic sympathectomy was done for angina . In fact ,  even in  CABG  , one of the the  mechanisms  for  angina  relief  is attributed  to cardiac denervation.

Caution: Even a small  episode of ischemia can trigger an electrical event .But it is rare.

 How common is silent infarct (STEMI) in diabetic patients ?

In a simple questionnaire we asked the diabetic patients in our CCU how they felt their pain during MI.Most felt it normally as do other non diabetic .  Diabetes  does not make  all anginal episodes  silent. Severe episodes of ischemia may be painful while less severe episodes may be painless. Diabetic autonomic neuropathy  is a  least recognized and  poorly understood complication of diabetes.Diabetes , involves  the vasanervorum of the autonomic nerves.

 The other mechanisms postulated in diabetic neuropathy are

  • Reduction in neurotrophic growth factors.
  • deficiency of essential fatty acids .
  • Reduced endoneurial blood flow and
  • Nerve hypoxia .

Is diabetic autonomic neuropathy treatable ?

Very difficult problem indeed.Controlling diabetes may partially correct  the neural dysfunction.Many add on neuro vitamins and aminoacids are having a good market !

If you successfully treat diabetic autonomic neuropathy will my patient  start feeling the  hitherto silent episodes of angina ?

We don’t know.Logic would answer ” YES”

What is the ultimate effect of cardiac autonomic neuropathy.

Cardiac denervation.  The manifestations  are

  • Tachycardia, exercise intolerance
  • Orthostatic hypotension

 

Silent Myocardial Infarction : A complete list

 

                                            The growth of medical science has been phenomenal .It is estimated , the quantum of break throughs  and development  in the  last  50 years  is   nearly equal  to  2000 years of evolution of our  knowledge  put together.  Along with this growth , came the  unavoidable misuse , and abuse of medical science. This  is mainly due to contamination of medicine with commerce . Federal drug authority (FDA) and it’s variants  were formed in all countries to monitor the proper usage of  these technologies for the benefit of mankind. It has an authority to ban a drug or device  , if it is found to bring more injury or side effects  than benefit !

But , unfortunately there is no legal authority to ban an  an  investigation  which is  potentially  or (really  harmful )

or  used  extensively without any valid purpose .

The list of such investigation is increasing in every speciality 

In  cardiology

  • Doing a Troponin assay in patients wuth classical STEMI
  • MDCT in general population
  • Pro BNP in all suspected cardiac  failure
  • Routine C reactive protein for CAD
  • Central venous catheters for all pateints with shock.

Is there a case for banning an investigation (Like banning a drug) for the benefit of  our patients ?

Looking superficially , it  may seem  ironical. But we realise many seemingly  innocuous investigations are responsible for uncontrolled misery for many patients.

This especially true in people who throng the wellness clinic (Also called master health check up)

A incidentally high C – reactive protein   can lead on to forearm blood flow assessment of endothelial dysfunction and carotid intimal plaque  that could  lead onto carotid stents ! and life long anticoagulation , and an  excess INR and sudden cerebral bleed and death !

This is one sample story  in one particular speciality

There is a definite case for banning ( Either total or partial)  some of the questionable investigations  which are done routinely !

Just because these investigation do not have any  physical , visible , adverse reactions like a drug , it should not be allowed to be abused  .The consequence of  false positive results of these investigations could be terrible and worse than the real disese itself !

ecg-ventriculophasic-21

Ventriculophasic sinus arrhythmia is a non-respiratory sinus arrhythmia seen in complete AV block.

The PP interval enclosing a QRS complex is shorter than a PP interval not enclosing a QRS.

The Mechanism 

ecg-ventriculophasic-sinus-arrhytmia1

The proposed mechanism is the  increased blood flow into the SA node artery  during ventricular systole  stimulating it to produce an early pacemaker activity and thus shortening the sinus cycle length.

Clinical significance : None for the patient  Academic purpose for the students

coronary-artery1

                                                      Coronary arterial circulation is the life line for  the human heart  and it’s survival.Typically it is supplied by two coronary arteries,  left and right coronary artery.Both, together carry about  250ml of blood every minute.( Approxinately  equal to a  cup of  coke !  ).These coronary arteries  generally divide in a predetermined  fashion , and have multiple branches . It is a  mystery , what  decides this  branching pattern

Is it like a our palmar crease  ? or the cerebral gyri ?

However , it does follow a certain rule,  one major coronary artery  will follow the  four  important grooves of heart. In the left side ,  left main coronary artery (LM) originates in the left coronary sinus (Size varying between 1mm -20mm)  and usually bifurcates into LAD and LCX. The left anterior descending artery (LAD) runs in anterior interventricular  groove while ,  the right atrio ventriculo groove carries the right coronary artery(RCA) .Left  circumflex artery (LCX) traverses the  left atrio ventricular groove.The most inconstant branch is the posterior descending artery (PDA) which runs in the posterior interventricular  groove.PDA  can arise from either RCA, LCX or both or even from LAD.

The major branches of LAD are called diagonal and septal  while the branches of LCX are called obtuse marginal(OM).There can be two to three diagonal and OMs. 

What is ramus intermedius coronary artery ? What is the incidence of Ramus ?

The left main coronary artery  instead of bifurcating into two ,  it trifurcates into three vessels.(LAD, LCX, Ramus)

The real incidence could vary betweenn (10% to 30%) depending upon the series.

ramus

What course it takes ?

It generally goes in the angle between the LAD and the LCX.It may either behave like a large OM or a diagonal branch.It supplies the lateral free wall of the LV many times.The peculiarity of this vessel is it does not run in a anatomical groove .It simply slides over the free surface of LV.Rarely, a  very abnormal course of ramus,  criss cross the aorta and pulmonary artery .

How common is atherosclerosis within  Ramus ?

We don’t know yet. But it is very likely since it is an early branch from left main, it  might  have a  predilection for atherosclerosis  as like LAD or LCX ostium.In fact now we recognise more of  trifurcation lesions involving  three branches of left main .

What would be the ECG finding if a large ramus is the culpirit vessel during STEMI ?

This scenario could be rare.

ACS in ramus could  present as ST elevation in 1/Avl /V5,V6

  • Lateral MI
  • Apical MI
  • High lateral MI

But it is realised , whenever the ECG changes are not fitting with typical ASMI or a lateral MI one should suspect a ramus lesion

 What is the significance of ramus for an interventional cardiologist ?

ramus-2

                                                   PCI in ramus is a rare opportunity for a cardiologist .The issue here  is,  if ramus is involved  adjacent LAD and LCX is also likely to be involved .So it would logically be a multivessel , complex angioplasty.Isolated ramus lesion could be tackled easily.Another issue here could  be ,since this vessel is not within  any anatomical groove  stent deployment would have a poor  support and prone for mobilisation and migration .

Stents are mechanical  devices like  a  spring ,  used to  keep an artery open after a PTCA or PCI.

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                                Bare metal stents(BMS) were found to have restenois rate of about 25%.  So it was perceived a stent should have it’s own protective coat , so that it won’t get restenosed.For this the researchers thought  anti cancer drugs are ideal as they block cell proliferation and thus neovascualrisation and restenosis.Alas, they were found dismally wrong ,  after all , neointiaml proliferation is only a part of the problem of restenosis  and simple blocking of cell growth is insufficient . The issue doesn’t stop with that, the anti cancer drugs incorporated within the stent simply can not differentiate normal from abnormal cells and

DES effectively blocks the normal endothelisation over the stents and make this highly vulnerable for acute stent thrombosis .

This complication is unique to DES and can result in SCD.Further ,during the last 6 years of DES , we recognised the restenosis rate has increased form the much hyped O % to almost 15% and it’s still growing . These  complications  has made a huge question mark over the future of drug eluting stents !

des-coverage

The concept of DES may not die , but which drug it should elute should be answered ! This  again is  going to be a long battle. So it is currently   adviced,  based  on common sense ( With due respects to  those RCTs  funded by industry )

Whenever you encounter a block within the coronary artery* Ask the following  questions in sequence  ,

  • Whether we can leave it alone  with medical therapy  ,  if the answer is no , proceed  to the next step !
  • Is there a possibility for plain balloon angioplasty in a given vessel (POBA, Yes !  the concept is not dead yet !)
  • If you decide a stent is required , Will  the  bare metal  do the job ?
  • In multivessel CAD  , Did the issue of increased metal load on the  long term outcome was considered ?
  • If lesions appear complex,  should we  not strongly consider CABG as an option ?

However  if we  have the habit of  ask ing the following  question  you are likely to deviate from scientific approach  

Is it possible to put a stent  across  the block ?

Yes , will be the answer most of the time ,and the patient will invariably get one or more stents  and carry a life long  stent related problems.

*The rule does not apply in Acute coronary syndromes

Also read this letter  posted by the author published in  British medical journal

                                      One of the important principles of  post PCI care is,   we need  to be very careful  till the metal struts are fully endothelialised . This is of vital importance as improper endothelialisation  is a powerful trigger and nidus for a  imminent thrombosis and  acute coronary syndrome.

stent

It is a billion dollor irony , the much hyped DES does exactly what we don’t want ! and still it’s  usage is  increasing world wide .  The drugs (Anti cancer agents)  which coat the DES   are the villains as it  prevents  the  metal struts  from being endothelialised  and  keep the metal surface  raw and vulnerable , while the  much maligned  bare metal stents allow  this natural endothelialisation  process  without any interruption ! So right now it is mandatory  to administer dual antiplatelet agents  life long( life of the stent !)   for the patients with DES.

 Just look , at the following image of  a stent in vitro at  30 days follow up

des

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Let us not forget the basics !

  • HT management has been made  easier with the availability of  many  good drugs , at the same time it has become a complex  issue with as many classification and guidelines.
  • The management of HT has evolved over the decades. Now we have realised  HT  is not a simple number game . Reducing the blood pressure to target levels is not  sufficient and is not the primary aim !.
  • In fact we now know controlling the numbers alone is never going to work  , combined risk factor reduction is of paramount importance.
  • HT per se is less lethal but when it combines with hyperlipidemia and diabetes or smoking  it becomes  aggressive.The blood lipids  especially the LDL molecule  enjoy the high pressure environment  ,   penetrate and invade the vascular endothelium.
  • ASCOT  LLA  study has taught us,   for blood pressure reduction to  be effective and reduce CAD  events one has to reduce thier  lipid levels also.So , for every patient with HT there is not only a target BP but also a target LDL level .

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Final message

The tip for better vascular  health is  , all  hypertensive patients should keep their lipids to optimal levels and all hyperlipidemia patients should keep their BP as low as possible .

“Keep your LDL  as low as  your diastolic blood pressure  and  let us  keep it around 70 -80